In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I created The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

By Scott Adams

Published on 10/30/2003

Gastroenterology, Oct 2003, Vol 125, No 4, p1105-13
Celiac.com 10/30/2003 – It has long been

Gastroenterology, Oct 2003, Vol 125, No 4, p1105-13

Celiac.com 10/30/2003 – It has long been known that celiac disease
is caused by T-cell responses to wheat gluten-derived peptides, but
the toxicity of other widely consumed grains has not been well studied.
The researchers who conducted this study were aimed at determining the
toxic T-cell stimulatory properties of barley hordeins, rye secalins,
and oat avenins. Except for one instance, they found that there were
no identical T-cell stimulatory gluten peptide matches in these grains.
There were, however, similar responses found in "11 homologous
sequences in hordeins, secalins, and avenins located in regions similar
to those in the original gluten proteins," and seven of the 11
peptides were recognized by gluten-specific T-cell lines and/or clones
from patients with celiac disease. The team discovered that key amino
acids can be substituted, which will either partially or totally stop
the T-cell stimulation by the gluten peptides, and that "single
nucleotide substitutions in gluten genes will suffice to induce these
effects."

The researchers conclude: "These results show that the disease-inducing
properties of barley and rye can in part be explained by T-cell cross-reactivity
against gluten-, secalin-, and hordein-derived peptides. Moreover, the
results provide a first step toward a rational strategy for gluten detoxification
via targeted mutagenesis at the genetic level."